Nursing Care

If someone in your family needs regular nursing care, their doctor may be able to arrange for a community or district nurse to visit them at home. This will not, of course, be a sleeping-in arrangement but simply involves a qualified nurse calling round when necessary. If you want more concentrated home nursing you will have to go through a private agency. 

Consultus can sometimes supply trained nurses. Additionally, there are many specialist agencies that can arrange hourly, daily or living-in nurses on a temporary or longer-term basis. Terms of employment vary considerably. Some nurses will literally undertake nursing duties only – and nothing else; and may even expect to have their meals provided. Others will do light housework and act as nurse companions. 

Fees vary throughout the country, with London inevitably being most expensive. Private health insurance can sometimes be claimed against part of the cost, but this is generally only in respect of qualified nurses. Your local health centre or social services department should be able to give you names and addresses of local agencies. 

There may come a time when you feel that it is no longer safe to live entirely on your own. One possibility is to engage a companion or housekeeper on a permanent basis but such arrangements are normally very expensive. Permanent help can also sometimes be provided by agencies (such as those listed under ‘Temporary living-in help’), who will supply continuous four-weekly placements. 

This is an expensive option and the lack of continuity can at times be distressing for elderly people, particularly at the change-over point. But it can also lead to a happier atmosphere as the housekeeper comes fresh to the job and neither party has time to start getting on each other’s nerves.

Diagnosis of malignant mesothelioma

A definitive pathological diagnosis of malignant pleural mesothelioma usually requires a tissue (biopsy) specimen to demonstrate that the lesion has a mesothelial phenotype and that it shows neoplastic invasion, as opposed to benign entrapment of mesothelium as part of a fibro-inflammatory process. 

• Evidence of malignant mesothelioma on cytological examination of pleural effusion fluid should be confirmed by tissue biopsy or, if a biopsy is considered inadvisable, impractical, or unnecessary, the cyst diagnosis should be supported by clinical and radiological data as a surrogate for the histological demonstration of invasion. 

• The anatomical location and extent of the pleural tumor should be ascertained by imaging studies. 

• The histological appearances of malignant pleural mesothelioma can vary widely, from epithelioid, to sarcomatoid and biphasic mesotheliomas – together with distinctive subtypes – and such variation occurs not only from one mesothelioma to another but sometimes within single mesothelioma. 

• Recognition of the histological subtype can facilitate diagnosis and provides important prognostic information. 

• Immunohistochemistry is essential for the diagnosis and differential diagnosis of malignant pleural mesothelioma and should include positive and negative (carcinoma-related) markers.

The diagnosis of malignant mesothelioma can be difficult, with symptoms and clinical findings that can mimic and be mimicked by other diseases. Pleural mesothelioma patients may present with dyspnoea, chest pain (pleuritic or non-pleuritic), cough, weight loss, or any combinations of these symptoms. Initial clinical and radiological examination usually reveals a pleural effusion, often massive. 

Rarely, patients are asymptomatic at the time when a radiological abnormality is demonstrated, and patients seldom present with metastatic disease. Some patients with malignant mesothelioma experience a long interval between the first onset of symptoms and subsequent diagnosis, but whether a long interval signifies enhanced or diminished survival following diagnosis is unclear. 

Most patients with malignant pleural mesothelioma have a background of asbestos exposure, and some may have had antecedent symptoms associated with the benign asbestos-related disease – for example, symptoms related to asbestosis or benign asbestos pleuritis with effusion. Others may have radiological evidence of past asbestos exposure, such as pleural plaques. 

In general, biopsy, immunohistochemical analysis, and correlation with radiological and clinical features are needed for the diagnosis of mesothelioma. When immunohistochemical findings are non-diagnostic or discordant, electron microscopy – including electron microscopic examination of tissue retrieved from blocks of paraffin embedded biopsy tissue or cytology cell blocks – can be used, but electron microscopy is not recommended for ‘routine’ diagnosis of mesothelioma. 

Although several cytological and histological findings may raise varying levels of suspicion of malignant pleural mesothelioma a current requirement for the definitive clinicopathological diagnosis of malignant pleural mesothelioma is the demonstration of neoplastic invasion – for example, infiltration into subpleural fat, chest wall skeletal muscle, rib or lung – by histological examination or by imaging studies, and by the clinical exclusion of alternative causes for an atypical mesothelial proliferation. 

A component of malignant mesothelioma in situ can be diagnosed when invasion has been demonstrated in the same or different biopsy or by imaging studies. This applies specifically to epithelioid malignant mesotheliomas. Sarcomatoid malignant mesotheliomas are rarely diagnosable from effusion fluid cytology and are usually identified histologically, by the demonstration of invasion or overtly sarcomatoid areas.

What are Cyanogenic Glycosides?

Cyanogenic glycosides are chemical compounds that occur naturally in many plants, including species of Prunus (wild cherry), Sambucus (elderberry), Manihot (cassava), and Linum (flax), Bambusa (bamboo), and Sorghum (sorghum). Chemically, they are defined as glycosides of the a-hydroxynitriles. 

These compounds are potentially toxic as they are readily broken down by enzymic hydrolysis to liberate hydrogen cyanide when the plant suffers physical damage. Occurrence in Foods There are approximately 25 known cyanogenic glycosides, and a number of these can be found in the edible parts of some important food plants. 

These include amygdalin (almonds), dhurrin (sorghum), lotaustralin (cassava), linamarin (cassava, lima beans), prunasin (stone fruit), and taxiphyllin (bamboo shoots). Some of the main food sources of cyanogenic glycosides and their estimated potential yield of hydrogen cyanide are released on hydrolysis. Bitter apricot kernels have been marketed as a health food in the UK and elsewhere. They can contain high levels of the cyanogenic glycoside amygdalin.

Effects on Health

The toxicity of a cyanogenic plant depends largely on the amount of hydrogen cyanide that could be released on consumption of the plant. Adequate processing or preparation is required to ensure that detoxification of the food is complete before consumption. However, if the processing or preparation is insufficient to ensure detoxification, the potential hydrogen cyanide concentration released during consumption can be high. 

Upon consumption of the food, the enzyme b-glycosidase will be released and hydrolysis of the cyanogenic glycoside will commence, resulting in hydrogen cyanide formation. Certain gut microflora also produces b-glycosidases, which can contribute to the breakdown of cyanogenic glycosides into hydrogen cyanide. Hydrogen cyanide is cytotoxic and blocks the activity of cytochrome oxidase – an enzyme critical for cellular respiration. 

When cytochrome oxidase is blocked, ATP production stops, and cellular organelles cease to function. However, cyanide is readily detoxified in animals as all animal tissues contain the enzyme rhodanese – a thiosulfate sulfurtransferase enzyme that converts cyanide to thiocyanate, which is then excreted in the urine. Acute poisoning only occurs when this detoxification mechanism is overwhelmed. 

The symptoms of acute cyanide poisoning include rapid breathing, drop in blood pressure, raised pulse rate, dizziness, headache, stomach pains, vomiting, diarrhea, confusion, twitching, and convulsions. In extreme cases, death may occur. The minimum lethal dose of hydrogen cyanide taken orally is approximately 0.5–3.5 mg/kg body weight or 35–245mg for a person weighing 75 kg. The chronic effects of cyanide consumption are associated with regular long-term consumption of foods containing cyanogenic glycosides in individuals with poor nutrition. 

These effects are most notable in the tropics, where cassava, and to a lesser extent, sorghum, bamboo shoots, and lima beans are staple components of human diets. 

Malnutrition, growth retardation, diabetes, congenital malformations, neurological disorders, and myelopathy are all associated with cassava-eating populations subject to chronic cyanide intake. There are a number of documented cases of poisoning caused by the consumption of apricot kernels. One report concerned a 41-year-old female found comatose after eating approximately 30 bitter apricot kernels, who eventually recovered after treatment. 

There are also case reports of children being poisoned after consumption of wild apricot kernels and where the kernels were made into sweets without proper processing. The UK Committee on Toxicity recommended in March 2006 that a tolerable daily intake (TDI) of 20 mg cyanide/kg BW/day be applied, which is the equivalent of 1–2 bitter apricot kernels per day. There are over 2500 known species of plants that produce cyanogenic glycosides, usually in combination with a corresponding hydrolytic enzyme – a beta-glycosidase. 

When the cell structure of the plant is disrupted in some way, for example by predation, the beta-glycosidase is brought into contact with its substrate – the cyanogenic glycoside. This leads to the breakdown of the glycoside into sugar and a cyanohydrin, which rapidly decomposes to release hydrogen cyanide. The purpose of the reaction is to protect the plant from predation. Stability in Foods Cyanogenic glycosides break down when the cells of the plant are damaged, for example during preparation and processing, and release hydrogen cyanide. Hydrogen cyanide itself is not heated and stable and does not survive boiling and cooking processes. 

It can also be eliminated by fermentation. Processing Adequate processing of cyanogenic glycoside-containing plants should be sufficient to significantly reduce or remove the toxic agents prior to consumption. Processing procedures, such as peeling and slicing disrupt the cell structure of the plant so that b-glycosidases are released and the cyanogenic glycosides are hydrolyzed. 

Hydrogen cyanide is thus released and can be removed by cooking processes such as baking, boiling, or roasting. Fermentation is also used to remove hydrogen cyanide. These methods are particularly suitable for products such as cassava and bamboo shoots. There are two main types of cassava – bitter cassava and sweet cassava. The sweet variety contains a significantly lower concentration of cyanogenic glycosides than the bitter variety, and it is the sweet variety that is used commercially. 

Cassava is consumed largely as cassava flour, cassava chips, and tapioca pearls, all of which are processed products with a long history of safe consumption. Treatments for removing cyanogenic compounds from flaxseed include boiling in water, dry and wet autoclaving, and acid treatment followed by autoclaving. Solvent extraction has also been used to remove cyanogenic glycosides from flaxseed and oil. 

Legislation 

A safe level of cyanide in cassava flour for human consumption has been set by the WHO at 10 ppm. Low levels of cyanide are also present in almonds, sweet apricot kernels and in the stones of other fruit such as cherries, as well as in bitter apricot kernels. In the UK, the maximum level of cyanide that can be present as a result of using such materials as flavourings is regulated under the terms of the Flavourings in Food Regulations 1992 (as amended).