Wilderness and Rescue Medicine 7th Edition Jeffrey Isaac, PA-C and David E. Johnson, MD

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Section II: Critical Body Systems

The rapid onset of increased ICP from severe illness or injury will be fatal in most backcountry or offshore situations. Cardiopulmonary arrest due to severe brain damage does not respond to CPR or defibrillation. It is the early recognition of slow-onset swelling from the accumulation of edema fluid or slow bleeding that can save lives. Non-Traumatic Brain Injury Non-traumatic mechanisms that can lead to increased ICP include high altitude cerebral edema (HACE), hypoxia, stroke, infection, and hyperthermia. In essence, any problem that injures brain tissue can stimulate an inflammatory response and cause blood or exudate to accumu- late inside the cranium.

is significant because it carries the anticipated problem (A’) of increased ICP. Even if no seri- ous problem yet exists worrying about increased ICP can cause major safety and logistical issues in the remote setting. This is another case where a conscientious patient survey, careful monitor- ing, and good risk/benefit judgement will lead to the best plan. Assessment of TBI We cannot directly examine the brain in the field, at least in a living patient. Our assessment must be based on the mechanism of injury, estimating the force involved, and observing brain function. Generally, the less profound the signs and symp- toms are, the less severe the injury is and the less likely the brain is to swell. Conversely, an impres- sive mechanism with a lot of force and profound changes in brain function indicates a high prob- ability of significant brain injury. The common sign of altered mental status immediately after a blow to the head is a symp- tom of the initial injury, not evidence of increased ICP. A rapid return to normal mental status, even after a period of unconsciousness, would suggest mild injury very unlikely to result in a significant increase in ICP. This patient may not remember the accident but will remember everything before and after, and remains oriented to person, place, purpose, and time. In the absence of other com- plications, this would be considered a low risk TBI.

Non - Traumatic Brain Injury A’: Increasing ICP

General Principles

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• Stroke • Hyperthermia • Hypoxia • Electricity • Infection • Exercise Associated Hyponatremia • Altitude (HACE) • Neuro Toxins

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Sometimes, as with an ischemic stroke or electrical injury, altered mental status is just a symptom of the initial brain injury. There is no associated headache or vomiting unless the antici- pated problem of elevated intracranial pressure actually develops. That is why persistent altered mental status carries the anticipated problem of elevated intracranial pressure, unless the cause is known to be unrelated (e.g. chronic dementia, alcohol intoxication). Traumatic Brain Injury Traumatic brain injury (TBI) is the common term for brain injury from trauma. The terms head injury and concussion are also used but are less clear in meaning. The diagnosis of TBI

Traumatic Brain Injury

General Principles

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Field Assessment: • Any degree of amnesia • Any change in mental status • A’ is increased ICP and Brain Failure • Other terms include: • Concussion • Brain Trauma • Closed Head Injury

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Amore severe injury is evidenced by prolonged changes in mental status, loss of memory for the hours or days before the event, or persistent lapses