How is a medically induced coma triggered?
Fears after waking up
Fears after waking up
by Hannelore Gießen, Munich
The treatment of a life-threatening illness in the intensive care unit is a borderline experience that is also associated with strong stress reactions. For many patients, the experiences lead to deep-seated fears. Doctors are trying to prevent this with new pharmacological concepts.
“You don't need to go there. He won't notice anything anyway, ”was the motto years ago when a clinic chaplain wanted to visit a coma patient in the intensive care unit. Today we know that an unconscious person also communicates with his environment. Tiny signals tell hospital chaplain Thomas Kammerer that the patient is reacting while he is talking to him: The breath becomes calmer, the eyes under the closed lids move like someone who dreams. "A person's chances of survival are worse if they are only treated medically," the Catholic theologian is certain. "Every intensive care patient needs a person who believes in him," adds his Protestant colleague Peter Frör.
Later, people often remember the pastor's visit. So what do they get when their consciousness is turned off? The interdisciplinary conference “Traumland Intensive Care Unit”, which recently took place in Munich, investigated this question. Theologians, doctors, psychologists and nursing staff have pooled their experiences.
The observation of experts, but also relatives, that coma patients send signals through their bodies is now supported by neurobiological examinations. They show that islands of perception remain in people in altered states of consciousness.
Fears as long-term damage
"Many people who had traumatic experiences during their time as intensive care patients were significantly impaired in their quality of life even years later," said Professor Dr. Gustav Schelling from the Ludwig Maximilians University in Munich. Since 1994, doctors at the Clinic for Anaesthesiology at the University Hospital Munich-Großhadern have been researching how intensive care measures affect the quality of life of patients. They found that 30 percent of them had post-traumatic stress disorder. Fear, anxiety, shortness of breath paralyzed activity and joie de vivre, recurring images vehemently pushed their way into consciousness.
But the less delusional and the more concrete a patient has of his time in a coma, the less likely he will develop such a mental illness, the anesthesiologist reported. That is why intensive care physicians now place great value on the fact that a patient who leaves the intensive care unit knows where he has been, what has happened and which phases of the illness he has experienced.
In order to prevent post-traumatic stress disorders, doctors try to switch off consciousness as far as possible with sleeping pills and painkillers during intensive treatment. The longer a person is in a coma, the less successful this is. Pharmacological effects such as tolerance development are primarily responsible for this, explained Schelling. In addition, the central nervous system is activated by stress hormones, which can lead to a certain level of awareness.
The passage syndrome
Putting someone into a coma is easy, but not always bringing him back, Schelling explained. When a patient wakes up, he goes through different levels of consciousness. This can also lead to excessive reactions, such as a wake-up delirium: Patients become disoriented and begin to dream extensively, triggered by a rebound effect after stopping the sedatives, which suppressed the phases of Rapid Eye Movements (REM) during deep sleep.
A more recent study by the Munich University Clinic shows that patients who dream very intensely when they wake up are particularly often followed by recurring, fear-inducing images. There is a neurobiological explanation for this, Schelling explained: On the one hand, hallucinations and nightmares are triggered by inflammatory mediators such as the cytokine interleukin-2, which is released in massive amounts in severe generalized inflammation. On the other hand, the body is subjected to a violent stress reaction, in the course of which catecholamines such as adrenaline flood the organism. In the brain, these stress hormones activate the almond kernel area, part of the limbic system in which emotional memory is anchored. This means that what has been experienced is saved particularly intensively. Almost everyone is familiar with this mechanism whereby experiences that are associated with strong emotions are retained particularly well and for a long time in the memory. An example of this is September 11, 2001. Most people remember what they did when they saw the terrifying images of the collapsing towers.
Modified intensive therapy
Intensive care physicians are now drawing conclusions from these findings for the therapy: They modulate the stress reaction through a reduced and intermittent administration of benzodiazepines, so that the patients regularly wake up briefly and thus do not experience a week-long phase of unconsciousness.
In addition, many intensive care patients today are given hydrocortisone in low doses in order to interrupt the cascade of the so-called HPA (hypothalamus-pituitary-adrenal) stress axis. This three-part control circuit ultimately leads to the production of the steroid hormone cortisol. It fulfills a multitude of different tasks in the body. Complex processes in the brain such as attention, wakefulness and memory are also under the control of the adrenal cortex hormone. The hippocampus, which is important for the long-term storage of information, has a particularly large number of binding sites for cortisol. The increased amount of cortisol released during stress inhibits the processing of information in the hippocampus, whereby in-vitro studies have shown that the cortisol-induced memory blockade is primarily based on the fact that memories are poorly reproduced.
This effect is used in the protective administration of cortisol in coma patients to inhibit the recall of traumatic memories. While the administration of a beta blocker prevents traumatic experiences from digging deep into the memory as a memory trail, the corticosteroid blocks their constant reappearance. The administration of hydrocortisone is particularly indicated if etomidate has to be used as an emergency medication, since the drug inhibits the cortisol synthesis and its use often results in post-traumatic stress disorders. Therapy with the antipsychotic haloperidol also causes such psychiatric complications, so that Schelling recommended combining the substance with a benzodiazepine if possible.
The second pharmacological concept in the prevention of post-traumatic stress disorders uses propranolol to stop an adrenaline rush when the intensive care patient wakes up and thus prevent the experiences from being engraved in the memory. As the only active ingredient of the beta-adrenergic receptor inhibitors, propranolol crosses the blood-brain barrier and also acts in the central nervous system.
"We have drawn a further conclusion from the findings," said Schelling. "At the patient's bedside, we no longer talk about, but rather with him."
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