Meconium ileus equivalent (MIE) can be defined as a clinical manifestation in cystic fibrosis (CF) patients caused by acute intestinal obstruction by putty-like faecal material in the cecum or terminal ileum. A broader definition includes a more chronic condition in CF patients with abdominal pain and a coecal mass which may eventually pass spontaneously. The condition occurs only in CF patients with exocrine pancreatic insufficiency (EPI). It has not been seen in other CF patients nor in non-CF patients with EPI. The frequency of these symptoms has been reported as 2.4%-25%.

The treatment should primarily be non-operative. Specific treatment with N-acetylcysteine, administrated orally and/or as an enema is recommended. Enemas with the water soluble contrast medium, meglucamine diatrizoate (Gastrografin), provide an alternative form for treatment and can also serve diagnostic purposes. It is important that the physician is familiar with this disease entity and the appropriate treatment with the above mentioned drugs. Non-operative treatment is often effective, and dangerous complications following surgery can thus be avoided.

High Altitude Cerebral Oedema (HACE) is a severe and potentially fatal manifestation of high altitude illness and is often characterized by ataxia, fatigue, and altered mental status. HACE is often thought of as an extreme form/end-stage of Acute Mountain Sickness (AMS). Although HACE represents the least common form of altitude illness, it may progress rapidly to coma and death as a result of brain herniation within 24 hours, if not promptly diagnosed and treated.

HACE generally occurs after 2 days above 4000m but can occur at lower elevations (2500m) and with faster onset. Some, but not all, individuals will suffer from symptoms of AMS such as headache, insomnia, anorexia, nausea prior to transitioning to HACE. Some may also have concomitant High Altitude Pulmonary Oedema (HAPE). HACE in isolation is rare, but the absence of concomitant HAPE or symptoms of AMS prior to deterioration does not rule-out the presence of HACE.

Most cases develop as a progression of AMS and will include a history of recent ascent to altitude and prior complaints/findings of AMS including a headache, fatigue, nausea, insomnia, and/or light-headedness. Some may also have signs/symptoms of HAPE. Transition to HACE is heralded by signs of encephalopathy including ataxia (usually the earliest clinical finding) and altered mentation which may range from mild to severe. Other symptoms may include a more severe headache, difficulty speaking, lassitude, a decline in the level of consciousness, and/or focal neurological deficits or seizures.

The mainstay of treatment is the immediate descent of at least 1000m or until symptoms improve. If descent is not an option, one may use a portable hyperbaric chamber and/or supplemental oxygen to temporize illness, but this should never replace or delay evaluation/descent when possible. If available, dexamethasone 8mg for one dose, followed by 4mg every 6 hours should be given to adults via PO, IM, or IV routes.
Acetazolamide has proven to be beneficial in only a single clinical study. The suggested dosing regimen for Acetazolamide is 250 mg PO, given twice daily. Though effective in alleviating or temporizing symptoms, none of the adjunct treatment modalities are definitive or a replacement for an immediate descent.

In mild-to-moderate heroin overdoses, arterial blood gas (ABG) analysis reveals respiratory acidosis. In more severe overdoses, tissue hypoxia is common, leading to mixed respiratory and metabolic acidosis.

The normal range for PaCO2 is 35-45 mmHg (4.67 to 5.99 kPa). Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (i.e., >45 mm Hg) with an accompanying academia (i.e., pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (i.e., >30 mEq/L).

Arterial blood gases with pH = 7.31; pCO2 = 7.4 kPa; pO2 = 8.1 kPa would indicate respiratory acidosis.

Extrinsic allergic alveolitis (EAA) refers to a group of lung diseases that can develop after exposure to certain substances. The name describes the origin and the nature of these diseases:

‘extrinsic’ – caused by something originating outside the body
‘allergic’ – an abnormally increased (hypersensitive) body reaction to a common substance
‘alveolitis’ – inflammation in the small air sacs of the lungs (alveoli)

Symptoms can include: fever, cough, worsening breathlessness and weight loss. The diagnosis of the disease is based on a history of symptoms after exposure to the allergen and a range of clinical tests which usually includes: X-rays or CT scans, lung function and blood tests.

EAA is not a ‘new’ occupational respiratory disease and occupational causes include bacteria, fungi, animal proteins, plants and chemicals.

Examples of EAA include:

Farmer’s lung
This is probably the most common occupational form of EAA and is the outcome of an allergic response to a group of microbes, which form mould on vegetable matter in storage. During the handling of mouldy straw, hay or grain, particularly in a confined space such as a poorly ventilated building, inhalation of spores and other antigenic material is very likely.

There also appears to be a clear relationship between water content of crops, heating (through mould production) and microbial growth, and this would apply to various crops and vegetable matter, with the spores produced likely to cause EAA.

Farmer’s lung can be prevented by drying crops adequately before storage and by ensuring good ventilation during storage. Respiratory protection should also be worn by farm workers when handling stored crops, particularly if they have been stored damp or are likely to be mouldy.

Asthma is a condition characterized by airway hyperresponsiveness, which results in reversible increases in bronchial smooth muscle tone, and variable amounts of inflammation of the bronchial mucosa.
During an acute asthma attack, the already inflamed airways narrow further due to bronchospasm, which leads to increased airway resistance. Because of the increased smooth muscle tone during an asthma attack, the airways also tend to close at abnormally high lung volumes, trapping air behind occluded or narrowed small airways. Thus the acute asthmatic will breathe at high lung volumes, his functional residual capacity will be elevated, and he will inspire close to total lung capacity. The accessory muscles of respiration are often used to maintain the lungs in a hyperinflated state.

During episodes of acute asthma, pulmonary function tests reveal an obstructive pattern. This includes a decrease in the rate of maximal expiratory air flow (a decrease in FEV1 and the FEV1/FVC ratio) due to the increased resistance, and a reduction in forced vital capacity (FVC) correlating with the level of hyperinflation of the lungs. Because these patients breathe at such high lung volumes (near the top of the pressure-volume curve, where lung compliance greatly decreases), they must exert significant effort to create an extremely negative pleural pressure, and consequently fatigue easily. Overinflation also reduces the curvature of the diaphragm, making it less efficient in generating further negative pleural pressure.

A retrospective cohort study of the primary care records of 247 lung cancer patients diagnosed between 1998–2002 showed that 10% of the X-rays were reported as normal.
Other tests may include:
– Imaging tests: A CT scan can reveal small lesions in your lungs that might not be detected on an X-ray.
– Sputum cytology: sputum may reveal the presence of lung cancer cells.
– Tissue sample (biopsy): A sample of abnormal cells may be removed for histological analysis. A biopsy may be performed in a number of ways, including bronchoscopy, mediastinoscopy and needle biopsy. A biopsy sample may also be taken from adjacent lymph nodes.

COPD is commonly associated with progressive hypoxemia. Oxygen administration reduces mortality rates in patients with advanced COPD because of the favourable effects on pulmonary hemodynamics.

Long-term oxygen therapy improves survival 2-fold or more in hypoxemic patients with COPD, according to 2 landmark trials, the British Medical Research Council (MRC) study and the US National Heart, Lung and Blood Institute’s Nocturnal Oxygen Therapy Trial (NOTT). Hypoxemia is defined as PaO2 (partial pressure of oxygen in arterial blood) of less than 55 mm Hg or oxygen saturation of less than 90%. Oxygen was used for 15-19 hours per day.

Therefore, specialists recommend long-term oxygen therapy for patients with a PaO2 of less than 55 mm Hg, a PaO2 of less than 59 mm Hg with evidence of polycythaemia, or cor pulmonale. Patients should be evaluated after 1-3 months after initiating therapy, because some patients may not require long-term oxygen.

Bronchopneumonia presents as a patchy consolidation involving one or more lobes, usually the dependent lung zones, a pattern attributable to aspiration of oropharyngeal contents.

Symptoms of bronchopneumonia may be like other types of pneumonia. This condition often begins with flu-like symptoms that can become more severe over a few days. The symptoms include:
– fever
– a cough that brings up mucus
– shortness of breath
– chest pain
– rapid breathing
– sweating
– chills
– headaches
– muscle aches
– pleurisy, or chest pain that results from inflammation due to excessive coughing
– fatigue
– confusion or delirium, especially in older people

There are several factors that can increase your risk of developing bronchopneumonia. These include:
– Age: People who are 65 years of age or older, and children who are 2 years or younger, have a higher risk for developing bronchopneumonia and complications from the condition.
– Environmental: People who work in, or often visit, hospital or nursing home facilities have a higher risk for developing bronchopneumonia.
– Lifestyle: Smoking, poor nutrition, and a history of heavy alcohol use can increase your risk for bronchopneumonia.
– Medical conditions: Having certain medical conditions can increase your risk for developing this type of pneumonia. These include: chronic lung disease, such as asthma or chronic obstructive pulmonary disease (COPD), HIV/AIDS, having a weakened immune system due to chemotherapy or the use of immunosuppressive drugs.

An aspergilloma is a fungus ball (mycetoma) that develops in a pre-existing cavity in the lung parenchyma. Underlying causes of the cavitary disease may include treated tuberculosis or other necrotizing infection, sarcoidosis, cystic fibrosis, and emphysematous bullae. The ball of fungus may move within the cavity but does not invade the cavity wall. Aspergilloma may manifest as an asymptomatic radiographic abnormality in a patient with pre-existing cavitary lung disease due to sarcoidosis, tuberculosis, or other necrotizing pulmonary processes. In patients with HIV disease, aspergilloma may occur in cystic areas resulting from prior Pneumocystis jiroveci pneumonia. Of patients with aspergilloma, 40-60% experience haemoptysis, which may be massive and life threatening. Less commonly, aspergilloma may cause cough and fever.

The chance of two carriers of a recessive gene having a child that is homozygous for that disease (that is both genes are transmitted to the child) is 25%. Therefore, the chances of this couple having a child with CF are 25%(1/4) x 1/20 = 1/80.