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Biomedical subjects

K F Steinsiepe

Publications and source records attributed to K F Steinsiepe.

12 recordsLinked to original sources
PubMed1991

[Lateral intra- and extraforaminal lumbar disk hernia: clinical aspects and therapy].

Lateral lumbar disc herniations in or beyond the intervertebral foramen account for nearly 10% of all lumbar herniations. They affect the nerve root exiting at the same level. Such a lateral herniation of disc L4, for example, would impinge on nerve root L4, while a common herniation inside the spinal canal would compromise root L5. Myelography most often provides false-negative results. High-resolution CT scanning is completely accurate in demonstrating these lesions and therefore is considered the diagnostic method of choice. We review the anatomo-pathological and clinical features and propose guidelines for radiological examination of these herniations. Finally, the lateral microsurgical approach to the intervertebral foramen is described. It permits exposure of the lateral disc prolapse without opening the spinal canal or performing facetectomy.

False Negative Reactions↗
PubMed1990

[Acute and subacute leg and foot paralysis of radicular origin: clinical aspects, examination technique and differential diagnosis of root syndromes].

We describe symptoms and physical findings consistent with acute or subacute radicular lesions in the lower limb: radicular pain syndromes in the leg and the motor as well as sensory deficits of lumbar and sacral roots L2 to S1. We emphasize the importance of anterior thigh pain which is not sufficiently known, and we point out our neurological findings which do not correspond to descriptions in standard textbooks. Aids to the examination of these radicular syndromes are given, stressing the technique of examining motor signs. We also discuss the differential diagnosis to other, nonradicular syndromes and we present practical guidelines. Finally, surgical emergencies of practical importance are pointed out.

Adult↗
PubMed1989

Anticoagulation-related intracranial extracerebral haemorrhage.

From January 1981 to June 1986 116 patients with anticoagulation-related intracranial haemorrhage were referred to hospital. Seventy six of these haemorrhages were extracerebral, 69 were in the subdural and seven in the subarachnoid space. No epidural haemorrhages were identified. Compared with non-anticoagulation-related haematomas, the risk of haemorrhage was calculated to be increased fourfold in men and thirteenfold in women. An acute subdural haematoma, mostly due to contusion, was more frequently accompanied by an additional intracerebral haematoma than a chronic subdural haematoma. Trauma was a more important factor in acute subdural haematomas than in chronic. Almost half of the patients (48%) had a history of hypertension, more than a third (35%) had heart disease and about one fifth (18%) were diabetic. Headache was the most frequent initial symptom. Later decreased level of consciousness and focal neurological signs exceeded the frequency of headache. Three patients with subarachnoid haemorrhage and nine patients with acute subdural haematomas died, while those with chronic subdural haematomas all survived and had at the most mild, non-disabling sequelae. Myocardial infarction (22%), pulmonary embolism (20%), and arterial disease (20%) were the most frequent reasons for anticoagulant treatment. Critical review based on established criteria for anticoagulation treatment suggests there was no medical reason to treat a third of these patients. The single most useful measure that could be taken to reduce the risk of anticoagulation-induced intracranial haemorrhage would be to identify patients who are being unnecessarily treated and to discontinue anticoagulants.

Aged↗
PubMed1981

The course of chronic subdural hematomas after burr-hole craniostomy and closed-system drainage.

A consecutive series of 32 adult patients with chronic subdural hematoma was studied in respect to postoperative cerebral reexpansion (reduction in diameter of the subdural space) after burr-hole craniostomy and closed-system drainage. Patients with high subdural pressure showed the most rapid brain expansion and clinical improvement during the first 2 days. Nevertheless, a computerized tomography (CT) scan performed on the 10th day after surgery demonstrated persisting subdural fluid in 78% of cases. After 40 days, the CT scan was normal in 27 of the 32 patients. There was no mortality and no significant morbidity. Our study suggests that well developed subdural neomembranes are the crucial factors for cerebral reexpansion, a phenomenon that takes at least 10 to 20 days. However, blood vessel dysfunction and impairment of cerebral blood flow may participate in delay of brain reexpansion. It may be argued that additional surgical procedures, such as repeated tapping of the subdural fluid, craniotomy, and membranectomy or even craniectomy, should not be evaluated earlier than 20 days after the initial surgical procedure unless the patient has deteriorated markedly.

Adult↗
PubMed1975

[Clinical and experimental contribution concerning the pathogenesis of acute life-threatening complications during neck anaesthesia].

Apart from the usual hazards of local anesthesia (toxic reaction due to overdose or intravasal administration, allergic reaction, reaction to the vasoconstrictor), a further risk which should be borne in mind in local anesthesia of the neck region is inadvertent epidural or intrathecal administration of the local anesthetic agent. Depression of respiration or total respiratory failure may occur due to blockade of the superficially located medullary chemoreceptors in the form of a high or total spinal block. The pathogenesis of these incidents is investigated. Respiratory failure is usually reversible and requires immediate and effective therapy (artificial respiration, oxygen administration). The indications for neck anesthesia and their relativity within the entire therapeutic program should be given careful consideration. If (radicular) pain occurs during the injection, or if cerebrospinal fluid is aspirated, the procedure should be interrupted immediately and some time allowed to elapse. In fatal cases the injection channel must be dissected layer-wise in local anemia down to the dural sac. The possible pathway of toxic administration (epidural, subdural, intravasal) must be demonstrated chemically.

Acute Disease↗