During the day and at night SPL always surpasses the permissible noise exposure for 24 h of 45 db(A) recommended by the US Environmental Protection Agency. Alarms cause the most irritating noise. Hospital management should pay attention to internal noise, and SPL should be measured routinely.

Patients with severe craniocerebral trauma (sCCT) display metabolic and endocrine changes. The question is raised whether hormonal patterns give cues to the prognosis of outcome or not. In 21 patients the function of the adrenocortical, gonadal, thyroid and human growth hormone (hGH)-insulin system was assessed. LH, FSH, TSH, prolactin and hGH were stimulated. 3 groups of patients were formed. Group I: patients in acute phase with a Glasgow Coma Score (GCS) more than 6 (group Ia) and less than 6 (group Ib). Group II: patients in transition to traumatic apallic syndrome (TAS). Group III: patients with full-blown or resolving TAS. The values of group Ia comprised low T3, T4 and testosterone, elevated insulin, normal hGH. Group Ib had hypothyroid T3 and T4 and an attenuated response of LH, TSH, prolactin and hGH to stimulation. Group III: there was seen an endocrine normalisation with elevated T4 and TBG and an altered response of hGH and prolactin to stimulation. Endocrine abnormalities were not helpful in predicting which course, either to better or to worse, a given patient would follow.

The activity of the sympathetic nervous system during the course of severe closed head injury has been evaluated in 15 patients by measuring plasma levels of epinephrine and norepinephrine. With the onset of the transition stage from midbrain syndrome to the apallic syndrome the plasma levels mainly of norepinephrine started to increase and remained high during the further course of the disease. During the remission from the apallic syndrome the elevated norepinephrine levels started to decline. The data indicate that a longlasting overactivity of the sympathetic nervous system is a characteristic feature in the course of severe head injury. As a rational therapy to protect the peripheral tissues against the consequences of a longlasting sympathetic overactivity we suggest the use of beta-adrenergic blocking agents and adrenergic neuron blocking drugs.

No abstract