Critical illness polyneuropathy
Under critical illness polyneuropathy ( CIP) is defined as a disease of the peripheral nervous system that often occurs in the context of severe, requiring treatment in intensive care diseases. Significant development factors are sepsis, multiple organ failure and long-term rescue breaths. This disease presents a neurological picture, which has been known for decades, but has long been misjudged.
Sepsis patients who were cared for long periods of time in intensive care units, partly developed distinct forms of muscle atrophy ( muscle atrophy ). We suspected that the immobilization of the patient leads to the intensive care unit to a disuse atrophy of muscle tissue and thus the clinical picture would be explained. However, this falls short. The complaints of the patients can thus not satisfactorily explain. Rather, a new disease to acquired in this process seems to participate. These are now known under the name " critical illness polyneuropathy ".
The incidence of this disease is underestimated. Approximately 70 percent of patients treated for one to two weeks in intensive care units against sepsis and survive, develop a CIP.
Pathology
The exact origin ( pathogenesis ) of the CIP is still not known. It is believed that inflammatory mediators play ( cytokines, interleukins, etc. ), ( SIRS ) are being channeled by the immune system in the body as in sepsis and the systemic inflammatory response syndrome, a crucial role in the genesis. This to date is very incompletely classified mediators appear to have a toxic effect on the axons specifically to exercise the motor neurons of the peripheral nervous system as part of the CIP. It therefore is an endogenously -toxic polyneuropathy. The damage to the motor neurons leads to paresis (paralysis ) of the attached muscles. The consequence of this is their atrophy. Sensory neurons appear largely, but not completely, to remain spared in this disease process. The progressive form of the CIP is monophasic and self-limiting.
Symptoms
The patients developing severe, flaccid, atrophic paralysis. All extremities are affected. The problem is the involvement of the diaphragmatic nerve ( phrenic nerve ). This can be seen only rarely in the early stages of the disease, since most patients concerned are already artificially ventilated. In an attempt to wean the patient from mechanical ventilation, sometimes arise, however, considerable difficulties. It should be noted that the CIP in most cases, fortunately not reached the severity to cause said weaning disorders. Clinically detectable, this type of disease may be difficult. On neurological promulgate the mentioned muscle atrophy found with peculiar doughy Gewebskonsistenz. The tendon reflexes are greatly reduced or absent. Pain stimuli on the legs are not using a flexor reflex ( shortening reaction) answered, as would be expected physiologically, but manifest themselves only over a grimacing face. This is a fairly typical sign of the CIP, but has no pathognomonic character.
Diagnosis
The electrophysiological study is the method of choice. The corresponding findings in the CIP are typically near-normal nerve conduction velocities ( NCV ) and distal motor latencies with amplitude - impaired or enlarged compound action potentials. The sensitive NLGS are practically normal. Myasthenia gravis, botulism and Guillain- Barré syndrome are the classical differential diagnoses for CIP. These are in contrast to the CIP pharmacotherapy quite accessible and must be checked in every case.
Therapy
The treatment is purely supportive. Central is the treatment of the underlying disease of the patient. A causal therapy against the CIP does not exist today. There are various clinical experiments with NMDA antagonists. Tangible achievements were far from though.
Careful care is the prevention and minimization of pressure lesions ( decubitus) of pronounced importance. The spontaneous prognosis, however, is unexpectedly good. Survival of the patients, the underlying disease, win most of them over weeks and months, their motor skills for the most part back. A restitutio ad integrum is, at least from neurological side, probably. In the convalescent phase, a breathless supportive treatment with oxygen supplementation is often necessary.
Can be problematic prove the often very long respiration phase in these patients. Secondary complications such as pneumonia, sepsis tracheomalacia and a new set not insignificant problem of medical care dar.