Showing posts with label RESPIRATORY FAILURE. Show all posts
Showing posts with label RESPIRATORY FAILURE. Show all posts

Study: Arsenic Exposure In Womb Linked To Increased Respiratory Infections For Newborns

By Dr Deepu









HealthDay (11/23) reports that a new study published in the journal Environmental Health Perspectives suggests that children exposed to high levels of arsenic in the womb face an increased risk for infections and respiratory symptoms in the first year of their life. Researchers measured levels of arsenic in 412 pregnant women in New Hampshire whose homes and private wells, and they found “infants exposed to arsenic in the womb had more infections that led to a doctor visit or treatment with prescription medications.” senior author Margaret Karagas, chair of epidemiology at Dartmouth College’s School of Medicine, said in a college news release: “These results suggest that arsenic exposure may increase the risk and severity of certain types of infections.”

Read about ARSENIC and its permissible limits

RESPIRATORY FAILURE

Pulmonary Medicine blog

Respiratory failure occurs when the respiratory system fails in oxygenation and/or carbon dioxide (CO2) elimination. Respiratory failure may be:[1]
  • Hypoxaemic respiratory failure (type I respiratory failure): PaO2 is less than 60 mm Hg (8 kPa) with a normal or low PaCO2. This is caused by ventilation-perfusion mismatch with either/both:
    • Under-ventilated alveoli (eg pulmonary oedema, pneumonia or acute asthma).
    • Venous blood bypasses ventilated alveoli (eg right to left cardiac shunts).
    Hyperventilation increases CO2 removal but does not increase oxygenation, as blood leaving unaffected alveoli is almost fully saturated.
  • Hypercapnic respiratory failure (type II respiratory failure): PaCO2 is more than 50 mm Hg (6.5 kPa) and indicates inadequate alveolar ventilation. Any ventilation-perfusion mismatch will affect PaO2 and therefore hypoxaemia is also common.
Respiratory failure may be acute or chronic:[2]
  • Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually therefore less than 7.3.
  • Chronic respiratory failure develops over several days or longer. There is sufficient time for renal compensation and an increase in bicarbonate so the pH is usually only slightly decreased. Clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale.

Common causes of type I respiratory failure

  • Chronic obstructive pulmonary disease (COPD).
  • Pneumonia.
  • Pulmonary oedema.
  • Pulmonary fibrosis.
  • Asthma.
  • Pneumothorax.
  • Pulmonary embolism.
  • Pulmonary hypertension.
  • Cyanotic congenital heart disease.
  • Bronchiectasis.
  • Acute respiratory distress syndrome.
  • Kyphoscoliosis.
  • Obesity

Common causes of type II respiratory failure

  • COPD.
  • Severe asthma.
  • Drug overdose, poisoning.
  • Myasthenia gravis.
  • Polyneuropathy.
  • Poliomyelitis.
  • Muscle disorders.
  • Head injuries and neck injuries.
  • Obesity.
  • Pulmonary oedema.
  • Adult respiratory distress syndrome.
  • Hypothyroidism.
The cause of respiratory failure is often clear from a thorough history and physical examination. See also the separate article Respiratory System - History and Examination.

Symptoms

  • The history may indicate the underlying cause, eg paroxysmal nocturnal dyspnoea, and orthopnoea in pulmonary oedema.
  • Both confusion and reduced consciousness may occur.

Signs

  • Localised pulmonary findings are determined by the underlying cause.
  • Neurological features may include restlessness, anxiety, confusion, seizures, or coma.
  • Tachycardia and cardiac arrhythmias may result from hypoxaemia and acidosis.
  • Cyanosis.
  • Polycythaemia is a complication of long-standing hypoxaemia.
  • Cor pulmonale: pulmonary hypertension is frequently present and may induce right ventricular failure, leading to hepatomegaly and peripheral oedema.
  • Arterial blood gas analysis: confirmation of the diagnosis.
  • CXR: often identifies the cause of respiratory failure.
  • FBC: anaemia can contribute to tissue hypoxia; polycythaemia may indicate chronic hypoxaemic respiratory failure.
  • Renal function tests and LFTs: may provide clues to the aetiology or identify complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ dysfunction.
  • Serum creatine kinase and troponin I: to help exclude recent myocardial infarction. Elevated creatine kinase may also indicate myositis.
  • TFTs (hypothyroidism may cause chronic hypercapnic respiratory failure).
  • Spirometry: useful in the evaluation of chronic respiratory failure.
  • Echocardiography: if a cardiac cause of acute respiratory failure is suspected.
  • Pulmonary function tests are useful in the evaluation of chronic respiratory failure.
  • ECG: to evaluate a cardiovascular cause; it may also detect dysrhythmias resulting from severe hypoxaemia or acidosis.
  • Right heart catheterisation: should be considered if there is uncertainty about cardiac function, adequacy of volume replacement, and systemic oxygen delivery.
  • Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic oedema.
A patient with acute respiratory failure generally needs prompt hospital admission in an intensive care unit. Many patients with chronic respiratory failure can be treated at home, depending on the severity of respiratory failure, underlying cause, comorbidities and social circumstances.
  • Immediate resuscitation may be required.
  • Appropriate management of the underlying cause.

Hypoxaemia

  • Ensure adequate oxygen delivery to tissues, generally achieved with a PaO2 of 60 mm Hg or an arterial oxygen saturation (SaO2) of greater than 90%.
  • Beware the prolonged use of high-concentration oxygen in chronic sufferers who have become reliant on their hypoxic drive to maintain an adequate ventilation rate. Elevating the PaO2 too much may reduce the respiratory rate so that the PaCO2 may rise to dangerously high levels.
  • Assisted ventilation:
    • Mechanical ventilation is used to increase PaO2 and to lower PaCO2. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue. Weaning patients with chronic respiratory failure off of mechanical ventilation may be very difficult.[2]
    • Non-invasive ventilation (NIV) has been increasingly used as an alternative to intubation. NIV improves survival and reduces complications for selected patients with acute respiratory failure. The main indications are exacerbation of COPD, cardiogenic pulmonary oedema, pulmonary infiltrates in immunocompromised patients, and weaning of previously intubated stable patients with COPD.[3]

Hypercapnia and respiratory acidosis

Correct the underlying cause and/or provide assisted ventilation.
  • Pulmonary: for example, pulmonary embolism, pulmonary fibrosis, and complications secondary to the use of mechanical ventilation.
  • Cardiovascular: for example, cor pulmonale, hypotension, reduced cardiac output, arrhythmias, pericarditis, and acute myocardial infarction.
  • Gastrointestinal: for example, haemorrhage, gastric distention, ileus, diarrhoea, and pneumoperitoneum. Duodenal ulceration caused by stress is common in patients with acute respiratory failure.
  • Polycythaemia.
  • Hospital-acquired infection: for example, pneumonia, urinary tract infections, and catheter-related sepsis, are frequent complications of acute respiratory failure.
  • Renal: acute kidney injury (acute renal failure) and abnormalities of electrolytes andacid-base balance are common in critically ill patients with respiratory failure.
  • Nutritional: including malnutrition and complications related to administration of enteral or parenteral nutrition. Complications associated with nasogastric tubes, eg abdominal distention and diarrhoea.
The mortality rate associated with respiratory failure depends on the underlying cause.

Further reading & references

  1. Roussos C, Koutsoukou A; Respiratory failure. Eur Respir J Suppl. 2003 Nov;47:3s-14s.
  2. Kaynar AM et al, Respiratory Failure, Medscape, Sep 2010
  3. Nava S, Hill N; Non-invasive ventilation in acute respiratory failure. Lancet. 2009 Jul 18;374(9685):250-9.

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