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Biomedical subjects

H Gjessing

Publications and source records attributed to H Gjessing.

4 recordsLinked to original sources
PubMed1998

Third degree obstetric tears; outcome after primary repair.

BACKGROUND: Disruption of the anal sphincter occurs in 0.5 to 2.5% of women during delivery. Defects of the sphincter are major causes of fecal incontinence. More than 30% of women who suffer from third degree perineal tears develop incontinence. We sought to determine the incidence of symptoms and injury to the anal sphincter among women who gave birth during a 5 year period. We also investigated the sensitivity of manometry and endosonography as well as the correlation of these two diagnostic modalities. METHODS: Thirty-eight women were examined one to five years after delivery. We used a questionnaire to assess symptoms of anal incontinence. Anal manometry and endosonography were performed. RESULTS: Twenty (57%) women had symptoms; most of them (34%) in the form of flatulence incontinence. The rest were incontinent of either liquid or solid stools. Four of these women were re-operated. Seventeen percent of the women suffered from anal incontinence during sexual intercourse. Only seven women had been in contact with a doctor regarding these problems. CONCLUSION: The fact that 57% of the women that took part in this study reported complications, leads us to the conclusion that the primary repair of third degree anal sphincter tears is unsatisfactory. It is important to decide whether any changes in primary repair may improve results in the future. Sexual dysfunction is also a complication of third degree obstetric tear with primary repair. It is important that the women who suffer from anal sphincter tear, as well as doctors, are given information about possible symptoms and the treatment available.

Adult↗
PubMed1989

Peripheral nerve function during hyperglycemic clamping in insulin-dependent diabetic patients.

The influence of hyperglycemia on peripheral nerve function was studied in 9 patients with long-term insulin-dependent diabetes. Blood glucose concentration was raised 13.5 +/- 0.5 mmol/l (mean +/- SEM) within 15 min and kept approximately 15 mmol/l over basal level for 120 min by intravenous glucose infusion. Hyperglycemia was accompanied by increased plasma osmolality. Sensory and motor nerve conduction and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min hyperglycemia. Distal (5th finger - wrist) and proximal (wrist - elbow) sensory nerve conduction showed an insignificant increase as hyperglycemia was induced. During hyperglycemia mean distal sensory conduction decreased from 53.1 m/s to 50.4 m/s (P less than 0.05) and mean proximal sensory conduction decreased from 56.0 m/s to 54.2 m/s (P less than 0.01). A mean of distal and proximal sensory conduction increased (53.5 m/s vs 54.6 m/s) (P less than 0.05) as hyperglycemia was induced and decreased (54.6 m/s vs 52.3 m/s) (P less than 0.01) during clamping. Motor nerve conduction decreased insignificantly throughout the study. Mean distal motor latency decreased from 3.1 ms to 2.8 ms (P less than 0.005) immediately after induction of hyperglycemia. During hyperglycemia it increased from 2.8 ms to 3.1 ms (P less than 0.001). We conclude that acute induction of hyperglycemia in long-term diabetics seems to increase sensory conduction and decrease distal motor latency, while 120 min hyperglycemia seems to decrease sensory conduction and increase distal motor latency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Peripheral nerve function during hyperglycemic clamping in healthy subjects.

The influence of hyperglycemia with physiological hyperinsulinemia on peripheral nerve function was studied in 10 non-diabetic subjects. Blood glucose concentration was raised from 3.8 +/- 0.2 mmol/l (mean +/- SEM) to 17.1 +/- 1.4 mmol/l (mean +/- SEM) within 15 min and kept at this level for 120 min by intravenous glucose infusion. Sensory and motor nerve conduction velocity, and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min of hyperglycemia. Mean sensory nerve conduction velocity increased from 57.7 m/s to 59.5 m/s (P less than 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s (P less than 0.05). An insignificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms (P less than 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms (P less than 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.

Adult↗