Environmental Emergencies
A 34 year old woman is brought to the Emergency Department by the local coastguard helicopter. She started complaining of chest pain and shortness of breath approximately 1 hour ago while surfacing from a dive. She has not lost consciousness at any point and denies any other symptoms. On examination you note decreased air entry in the right chest and crepitus of the neck. Her observations are recorded as:
- Heart rate: 95 beats/minute
- Blood pressure: 128/87 mmHg
- Respiratory rate: 22 breaths/minute
- Oxygen saturations: 97% on air
- Temperature: 36.7°C
A chest radiograph shows a right-sided pneumothorax and a pneumomediastinum. What is the management of this condition?
Answer:
This patient has suffered from pulmonary barotrauma. The treatment for a pneumothorax from pulmonary barotrauma is the same as for a pneumothorax from another cause—that is, aspiration, catheter insertion, or chest tube placement. Management of pneumomediastinum is supportive. Recompression is only necessary for decompression sickness (DCS) or arterial gas embolism (AGE), not for barotrauma.Decompression Illness
Environmental Emergencies
Last Updated: 10th May 2022
Decompression illness (DCI) is a disease of compressed gas divers, aviators, astronauts and caisson workers where gas bubbles form in tissues and/or the blood during or after a decrease in environmental pressure. In the United Kingdom (UK) this is most commonly seen in divers.
There are two types of decompression illness: decompression sickness (DCS) and arterial gas embolism (AGE).
Pathophysiology
Decompression sickness:
Decompression sickness is caused by nitrogen coming out of solution when a diver ascends from a dive. It is sometimes described as being caused by evolved gas. The inert gas that evolves from the tissues can then cause a mass effect and inflammatory response in that tissue. This can happen anywhere in the body but is commonly seen in the articular cartilage (joints) and nervous tissue especially the spinal cord.
The full mechanism and pathophysiology of DCS is poorly understood and still being researched. It is thought there are two main effects from evolved gas:
- Direct damage (primary). Direct damage to the tissue resulting from the gas bubbles is thought to be caused by artery occlusion, damage to vascular endothelium and venous outflow obstruction. The effects on the vessels results in a disturbance of vascular permeability and microvascular flow which can cause a breakdown in the blood brain barrier.
- Inflammatory response (secondary). Gas bubbles cause secondary effects by activating the clotting cascade, platelets, complement and leucocytes resulting in an inflammatory response in the affected tissues.
Due to these two mechanisms of tissue damage DCI can present anytime from 0-72 hours or more after a dive, although the majority of cases come on within 6 hours of a dive. The symptoms due to the direct effect of bubbles usually present quickly whereas inflammatory responses can cause a latent response. This also means that DCI can have an evolving course with inflammatory mediated symptoms worsening over time.
Arterial gas embolism:
Arterial gas embolism occurs when nitrogen bubbles escape in to the arterial circulation. This can result from a few different mechanisms:
- Pulmonary barotrauma. As per Boyle’s law, gas expands in volume as pressure decreases. Therefore the air in a divers lungs expands as the diver makes their way to the surface. If a diver doesn't equalise the pressure (holds their breath on ascent) or has an underlying pulmonary disease (causing gas trapping in the lungs) an over inflation injury can occur. Air from the pneumothorax can then embolise into the pulmonary circulation, and reach the left side of the heart, to then be pumped in to the systemic arteries.
- Patent foramen ovale/arteriovenous malformation (right to left shunt). Any bubbles in the venous circulation which may not normally cause a problem shunt in the arterial circulation and become an arterial gas embolism.
- Overwhelming the pulmonary filter. Most divers bubble after most dives - these bubbles usually diffuse into the alveoli where they are exhaled. If this filter is overwhelmed, for example due to exercise, the bubbles will pass through the lungs without being filtered out and will then pass in to the arterial circulation via the left heart.
The escaped gas (AGE) can then lodge anywhere in the arterial system, causing arterial occlusion and resulting ischaemia. The most serious form is when a gas embolus lodges in the cerebral arterial circulation known as a cerebral arterial gas embolus (CAGE). Due to the pathophysiology of AGE, symptoms usually have a quick onset and patients need swift recompression in order to reduce permanent irreversible damage caused by tissue ischaemia.
Risk factors
Risk factors for decompression illness:
- Deep dive, long dive, missed decompression stops, multiple dives
- Age
- Exercise during or after a dive
- Flying/ ascending to altitude after diving
- Obesity
- Dehydration
- Alcohol use prior to dive
Clinical features
Bubbles can form in or move to most parts of the body and so decompression illness can present with almost any clinical picture. Some of the more common presentations include:
- Limb or joint pain– often a toothache type pain, usually not worse on movement or palpation
- Girdle pain– pain coming from the back and spreading to the abdomen
- Neurological symptoms– tingling, numbness, weakness, change in behaviour or personality, poor coordination, loss of bowel or bladder control, changes in hearing or vision, memory loss, unconsciousness
- Chest pain or breathing difficulties– this could suggest a pneumothorax, gas within the coronary vessels or immersion pulmonary oedema
- Rash– often a mottled rash called cutis marmorata. This can precede a more severe neurological DCI
- Audiovestibular hearing loss, balance and coordination problems, vertigo and vomiting
- Constitutional symptoms– malaise, headache, lethargy, loss of appetite, apathy etc.
Decompression illness is primarily a clinical diagnosis and is assessed with a very thorough and detailed history and examination. A chest x-ray is often useful to assess for pulmonary barotrauma (pneumothorax, pulmonary oedema, subcutaneous emphysema), although further investigations may be required.
Management
- Call the National Diving Accident Helpline (or Divers Alert Network).
- Oxygen
- This is the most effective management of decompression illness in the emergency department. It improves prognosis and is usually all patients need in terms of analgesia. All patients should be started on high flow oxygen at 15 L/min via a non-rebreather mask regardless of their oxygen saturations.
- Fluids
- Have a very low threshold for giving IV fluids. Insert a catheter if there is any suspicion the patient may be in retention.
- Insert a chest drain if there is evidence of a pneumothorax.
- Recompression therapy
- It is imperative to call a diving physician for help as soon as possible. Patients with DCI need recompression therapy, and this should not be delayed.
- Recompression therapy is the definitive treatment of decompression illness and involves the patient being transferred to a dedicated facility. The patient is re-pressurised in a chamber breathing 100% oxygen at a high partial pressure.
- There are 3 main effects of recompression therapy:
- Bubble crushing: as per Boyle’s law, increasing pressure decreases the volume of bubbles
- Flushing out the nitrogen bubbles with oxygen
- Healing damaged tissue with hyperbaric oxygen
- N.B. Do not give Entonox under any circumstances to anyone who has recently dived as the nitrous oxide is highly soluble and will increase the inert gas load, making the symptoms of DCI worse. It can also expand within the air filled spaces of the body and cause barotrauma to the lungs, ears, sinuses or gut.
- N.B. Do not give pain killers unless you have a very long transfer to a chamber, and only after discussion with a diving doctor. NSAIDs and opioids should be avoided.
Inner-Ear Barotrauma (IEBT)
Mechanism of injury:
Barotrauma refers to injuries due to pressure changes. Boyle’s law states that pressure and volume are inversely proportional (P × V = k or P1V1 = P2V2). As the pressure decreases, the volume of gas increases and can damage gas-filled structures (sinuses, inner/middle ears, lungs, and intestines). The incremental changes in pressure (and therefore volume) are greatest at the surface, so barotrauma most commonly occurs near the surface (either at the beginning or at the end of a dive). Long or deep dives are not required for barotrauma.
Clinical features:
Symptom onset is usually sudden and often associated with ear equalisation issues. Symptoms of middle-ear barotrauma are often present, but their absence does not rule out inner-ear barotrauma. Vertigo is usually severe and accompanied by nausea and vomiting. Ear pain may or may not be present. Hearing loss, sometimes with tinnitus, may occur. The eyes might show nystagmus. A feeling of fullness in the ears (often the least of the diver’s complaints) is possible.
IEBT or Inner-Ear Decompression Sickness (IEDCS)?
It is important to distinguish between these two conditions because their treatments differ. The standard treatment for DCS of any kind is hyperbaric oxygen therapy in a recompression chamber. Recompression (or any pressure change) is contraindicated when inner-ear barotrauma is likely. Differential diagnosis between IEDCS and IEBT can sometimes be a challenge. While the symptoms are similar in both conditions, there are a few characteristics that might help during the assessment:
- IEBT is often preceded by failed equalization of middle-ear pressure, usually occurring at the beginning of a dive during descent as a result of difficulty equalizing, and symptom onset is usually very acute. There may be evidence of middle-ear barotrauma.
- IEDCS is often a more delayed symptom onset (many minutes to a few hours), usually occurring after a moderate to significant dive exposure as a result of failed decompression. Other forms of DCS, including cutaneous DCS may be observed.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
