Clinical Cases in Paramedicine. Группа авторов
and highlight all of the information that might concern you as a paramedic.
Case Progression
En route to hospital, the patient starts to become lethargic and complains of a headache and dizziness. On checking the patients carbon monoxide (CO) level, you notice it is much higher than expected. You administer high‐flow oxygen through a non‐rebreathe mask using 15 L of oxygen and transport the patient to the nearest Emergency Department with a pre‐alert call due to the smoke inhalation and potential for CO poisoning.
Patient assessment triangle
General appearance
Alert but no longer meeting gaze.
Circulation to the skin
Normal.
Work of breathing
Increased work of breathing – but improved since treatment provided.
SYSTEMATIC APPROACH
Danger
None at this time.
Response
Alert but becoming lethargic.
Airway
Clear.
Breathing
RR: 28. Wheeze resolving following interventions.
Circulation
HR: 128. Palpable radial. Capillary refill time 1 second.
Disability
Moving all four limbs.
Exposure
Normal temperature in the ambulance.
Vital signs
RR: 28 bpm
HR: 128 bpm
BP: 130/78 mmHg
SpO2: 97%
CO: 25 ppm
Blood glucose: not repeated
Temperature: not repeated
GCS: E3, V6, M5, 14/15
4 lead ECG: sinus tachycardia
1 Explain the significance of the soot in and around the mouth and nose. Soot in mouth and nose is suggestive of inhalation injury. The patient also has singed nasal hair and a hoarse voice, so there is the potential for airway burns that may lead to further complications as the airway starts to swell. The cough indicates the patient may have inhaled irritants, so be aware for signs of toxicity as well. Inhalation injury is the main cause of mortality in burn patients.
2 Why might SpO 2 monitoring be unreliable in this patient? What else could you measure?Pulse oximetry measures peripheral capillary oxygen saturation (SpO2) and the percentage of haemoglobin (oxygenated haemoglobin) compared to the total amount of haemoglobin. Carbon monoxide is one of the products of combustion and can affect patients exposed to smoke‐filled environments. CO diffuses across the alveoli in a similar way to oxygen, creating carboxyhaemoglobin, which has a much greater affinity with haemoglobin than oxygen (approx. 250 times greater). This reduces the ability of the haemoglobin to transport oxygen around the body. Pulse oximetry cannot distinguish between oxyhaemoglobin and carboxyhaemoglobin and SpO2 readings may be falsely elevated, making it challenging to accurately determine the severity of the patient. Some non‐invasive pulse oximetry devices can measure carboxyhaemoglobin saturation (SpCO) levels, although most are not validated and should be used as an adjunct to clinical decision making.End‐tidal carbon dioxide (EtCO2) would be another useful addition, as it would help detect any bronchospasm that may not be noted on auscultation.
3 What are the signs and symptoms of carbon monoxide poisoning? See Table 1.5.Table 1.5 Signs and symptoms related to carboxyhaemoglobin (COHb) level at time of exposure to carbon monoxideSource: Adapted from Curtis et al. (2019), p. 535.COHb level %Signs and symptoms0None10Frontal headache20Throbbing headache, shortness of breath on exertion30Impaired judgement, nausea, fatigue, visual disturbances, dizziness40Confusion, loss of consciousness50Seizures, coma60Hypotension, respiratory failure70Death
1 What additional questions might help you to determine the severity? Duration of time in the smoke‐filled room?Any prior history of respiratory problems, especially asthma?Any action taken to prevent inhalation (cloth or towel across mouth and nose, stayed low to floor to avoid fumes, etc.)?Any signs and symptoms associated with CO poisoning?Does patient smoke (smokers have a higher baseline reading of CO)?
References and further reading
1 Austin, M., Wills, K., Blizzard, L. et al. (2010) Effect of high flow oxygen on mortality in COPD patients in prehospital setting: Randomised controlled trial. BMJ, 341: c5462.
2 Australian Medicines Handbook (2020) Salbutamol. Adelaide: Australian Medicines Handbook Pty Ltd. https://amhonline.amh.net.au/chapters/respiratory‐drugs/drugs‐asthma‐chronic‐obstructive‐pulmonary‐disease/beta2‐agonists/salbutamol (accessed 14 January 2020).
3 Bendall, J. & Middleton, P. (2015) Pulmonary embolism. In Paramedic Principles and Practice ANZ: A Clinical Reasoning Approach (eds M. Johnson, L. Boyd, H. Grantham & K. Eastwood), Chatswood: Elsevier Australia, p. 313.
4 British Thoracic Society (2019) BTS/SIGN Guideline for the Management of Asthma. https://www.brit‐thoracic.org.uk/quality‐improvement/guidelines/asthma/ (accessed 29 June 2020).
5 Burns, E. (2019) ECG changes in pulmonary embolism, Life in the Fast Lane, 9 May. https://litfl.com/ecg‐changes‐in‐pulmonary‐embolism/ (accessed 30 January 2020).
6 Busti, A. (2015) The mechanism of oral contraceptive (birth control pill) induced clot or thrombus formation (DVT, VTE, PE). Evidence‐Based Medicine Consult. https://www.ebmconsult.com/articles/oral‐contraceptive‐clotting‐factors‐thrombosis‐dvt‐pe (accessed 15 January 2020).
7 Camilleri, T. (2020) Medical emergencies. In Fundamentals of Paramedic Practice, 2nd edn (eds S. Willis & R. Dalrymple), Hoboken, NJ: Wiley‐Blackwell, pp. 347–348.
8 Curtis, K., Ramsden, C., Shaban, R. et al. (2019) Emergency and Trauma Care, 3rd edn. Chatswood: Elsevier.
9 Hampson, N. (2012) Non‐invasive pulse CO‐oximetry expedites evaluation and management of patients with carbon monoxide poisoning. American Journal of Emergency Medicine, 30(9): 2021–2024.
10 Johnson, M. (2015) The inflammatory response. In Paramedic Principles and Practice ANZ: A Clinical Reasoning Approach (eds M. Johnson, L. Boyd, H. Grantham & K. Eastwood), Chatswood: Elsevier Australia, pp. 993–1000.
11 Joint Royal Colleges Ambulance Liaison Committee (2019) JRCALC Clinical Guidelines