Page 626 - ACCCN's Critical Care Nursing

Emergency Presentations 603

CARBON MONOXIDE POISONING
Carbon monoxide (CO) is a gaseous byproduct of incom- TABLE 22.10 Summary of assessment and
plete fuel combustion, and is present where there is a management of acid and alkali exposure
flame in a confined space with improper ventilation or
air exchange. Levels of CO can accumulate rapidly, and Nursing step Corrosive acids or corrosive alkalis
the gas is dangerous as it is colourless, odourless, tasteless Assessment l Burns to skin, mouth, pharynx or oesophagus
and non-irritating. 129-131 Common sources of CO are l Gastric irritation with nausea and vomiting
faulty radiant heaters, kerosene lamps, cooking stoves,
engine exhausts and fireplaces. Acute CO poisoning is the Management l Airway
most common form of successful poisoning in the USA, l Breathing
UK and Australia. 129-131 l Circulation
l Decontamination
Assessment, Monitoring and Diagnostics Prevent l Do not induce vomiting.
Haemoglobin has a 210–240 times greater affinity for CO absorption l Remove contaminated clothing.
than for oxygen, and shifts the oxygen–haemoglobin l Flush the skin with copious amounts of
water.
curve to the left (see Chapter 13). As CO displaces oxygen
from red blood cells, the patient experiences hypoxaemia Enhance l Administer chelating agents if they exist,
and hypoxia. 132-134 Headache, nausea and vague pains are elimination such as calcium gluconate for hydrofluoric
acid.
often experienced at onset of poisoning, with increasing
tiredness and sleepiness, difficulty concentrating, and Symptomatic l Protect burnt skin with sterile dressings.
failure to recognise the onset of poisoning. With higher management l Monitor respiratory status.
levels of inhalation, the patient may be tachypnoeic,
tachycardiac and experience loss of consciousness. A
characteristic red colour presents in the lips with skin
flushing. 132-134 The most important factors in determining oesophageal mucosa, presenting a risk for haemorrhage
CO poisoning are a history of exposure with an elevated and mediastinitis, and cardiac arrest as a result. 135-137 The
blood carboxyhaemoglobin level. 132-134 late sequelae of swallowing a corrosive substance involves
mucosal scarring with constriction and mechanical
Management obstruction of the oesophagus.
As CO is an inhaled toxin, the patient should be removed
from the contaminated environment to prevent further Assessment
absorption and allowed to breathe fresh air until 100% Physical findings are site-specific and relate to the type of
oxygen can be administered. Although this may be inef- exposure – ingestion, inhalation or contact (see Table
fective because of the bond between CO and haemoglo- 22.10). Ingested acids present as burns to the mouth and
bin, high-flow high-concentration oxygen administration pharynx. Patients who are able to vocalise complain of
134
will reduce the half-life of CO. Hyperbaric oxygenation pain, gastric irritation with vomiting and haematemesis.
is used to treat severe cases of CO poisoning, as pres- Fumes from an ingested substance may cause pneumoni-
surised oxygen reduces the half-life of the carboxyhaemo- tis. Contact with skin or the eyes is similar to other types
globin molecule and shortens the duration of effects. As of burns, with a sharply-defined blister or wound, inflam-
hyperbaric resources are not available at every facility, mation, pain and ulceration. Hypotension and cardiovas-
treatment depends on carboxyhaemoglobin serum levels, cular collapse are also possible when damage occurs to
time since exposure, transport time to the hyperbaric underlying vital structures. 135-137
chamber and the clinical symptoms of the patient. 132-134 Inhalation irritates respiratory tissues, producing direct
Patients should be monitored for adverse effects of damage, oedema and alterations in ventilation. Patients
hypoxia, as they may have convulsions, cardiac arrhyth- may initially experience coughing, choking, gasping for
mias and acid–base disturbances.
air and increased secretions. Evaluate for obvious tissue
CORROSIVE ACIDS injury, impaired respiratory function, and subsequent
effects of hypoxia and pulmonary oedema, which may
A range of substances have a similar ability to cause local occur up to 6–8 hours later. 135,137 Arterial blood gases,
tissue injury. Common acids involved in toxic emergen- ventilation studies, serial chest X-rays and frequent physi-
cies include acetic acid (vinegar); carbolic acid (phenol cal assessments are used to monitor for changes.
disinfectants); chlorine (swimming pools, sanitising
agents); hydrochloric acid (pools, cleaning agents); Management
hydrofluoric oxalic (laundry agents); sodium bisulphate
(toilet cleaning agents; converts to an acid when added Contaminated clothing should be removed to prevent
to water) and sulfuric acid (car battery acid). recontamination. Patients with external contamination
should be washed thoroughly to remove any remaining
Ingested corrosives produce immediate or late life- surface material that may come into contact with treating
threatening complications. In general, acids dissolve staff. For acid contact with skin or eyes, begin immediate
tissue and destroy haemoglobin. 135 Swallowing a strong flushing with a non-reactive liquid and continue to do so
acid can produce ulceration and perforation of oral and for at least 15 minutes to guarantee complete removal. In