Diurnal blood pressure and urine production in acute spinal cord injury compared with controls.

STUDY DESIGN: This is a prospective observational study. OBJECTIVES: The objective of this study was to determine time-dependent changes in diurnal blood pressure (BP) and urine production in acute spinal cord injury (SCI). SETTING: This study was conducted in a specialist, state-based spinal cord service in Victoria, Australia. METHODS: Consenting patients admitted consecutively with acute SCI were compared with patients confined to bed rest while awaiting surgery and with mobilising able-bodied controls. Participants underwent ambulatory BP monitoring (ABPM), measurement of diurnal urine production and rated orthostatic symptoms over 1 year. Participants with night:day systolic BP (SBP) <90% were classified as dippers, 90-100% as non-dippers and >100% as reverse dippers. RESULTS: Participants comprised tetraplegics (n=47, 40.0±17.3 years), paraplegics (n=35, 34.4±13.9 years), immobilised (n=18, 30.9±11.3 years) and mobilising (n=44, 33.1±13.5 years) controls. At baseline, 24-h BP was significantly lower in tetraplegics (111.8±1.9/62.1±1.1 mm Hg) but not in paraplegics (116.7± 1.4/66.0±1.1 mm Hg), compared with controls (117.1 ±1.3/69.1±1.1 mm Hg), adjusting for gender. This difference was not observed at 1 year. The average night:day SBP in mobilising controls was 86.1±0.7%, differing from paraplegics (94.0±1.5%, P<0.001) and tetraplegics (101.5±1.5%, P<0.001). Urine production in tetraplegics and paraplegics did not fall at night compared with the day. Abnormal diurnal BP and orthostatic symptoms in tetraplegics persisted throughout the study. Nocturnal hypertension was observed in 27% (n=9) of tetraplegics, of whom only 2 had day hypertension. All mobilising controls with nocturnal hypertension (n=6, 14%) had day hypertension. CONCLUSION: People with SCI have a high prevalence of isolated nocturnal hypertension, reverse dipping, orthostatic intolerance and nocturnal polyuria. Cardiovascular risk management and assessment of orthostatic symptoms should include ABPM.

Management of Sedation and Paralysis.

Sedatives are administered to decrease patient discomfort and agitation during mechanical ventilation and to maintain patient-ventilator synchrony. Titration of infusions and or bolus dosing to maintain light sedation goals according to validated scales is recommended. However, it is important to consider deeper sedation for patients with refractory patient-ventilator dyssynchrony (PVD) to prevent volutrauma and barotrauma. Deep sedation plus muscle relaxants may be required to treat PVD or to reduce oxygen consumption and carbon dioxide production. Although minimization and protocolization of sedation in the intensive care unit improves costs and outcomes, it is important to consider goals on an individual basis.

Delayed hypokalemic paralysis following a convulsion due to alcohol abstinence.

We encountered three patients with hypokalemic paralysis following a convulsion in the early stages of alcohol abstinence. The transtubular potassium gradient was less than 2.0, suggesting intracellular potassium shift. Hypokalaemic paralysis may result from retention of intracellular cationic potassium bound by anionic phosphorylated compounds, precipitated by an acceleration of the (Na+)-(K+) pump in alcohol withdrawal and convulsions. These findings warn of the lethal hypokalemia that may occur after convulsions, particularly soon after alcohol abstinence associated with moderate withdrawal symptoms.

Search for new urinary biochemical markers of collagen degradation in man.

BACKGROUND: In the human body, collagen degradation produces various fragments released from the extracellular matrix, which end up in the urine as pyridinium cross-links, either free or bound to peptides or sugars. METHODS: We developed a high-performance liquid chromatography (HPLC) technique, which measures not only free pyridinoline (Pyr) and deoxypyridinoline (Dpyr), but also glucosyl-galactosyl-pyridinoline (glc-gal-pyr) and four still unidentified bound pyridinolines. Assuming that in Paget's disease of bone and in growing children the cross-links (CL) mainly originate from bone tissue, whereas after spinal cord injury their high excretion rather reflects the degradation of non-osseous collagen, we compared the urinary output of seven different cross-links, among which four had not been described before. RESULTS: Our results show that one of those, which we called CL1, is essentially originating from bone and is more specific in this respect than Dpyr, whereas glc-gal-pyr also reflects the degradation of non-osseous collagen. The best indicator of non-bone collagen degradation was CL3, one of the newly discovered cross-links. CONCLUSIONS: In conclusion, we demonstrate that new sensitive pyridinoline cross-links can be identified and assayed in human urine and that their specificity helps to distinguish diseases related to bone collagen from those in which other forms of collagen are involved.

Urinary free cortisol excretion shortly after ischaemic stroke.

The cortisol axis and catecholamine excretion were studied in 20 patients within the first week after acute ischaemic stroke. Urine free cortisol and plasma cortisol levels after dexamethasone were significantly higher in stroke patients than in 80-year-old volunteers (n = 32; P = 0.03 and P = 0.003, respectively). Catecholamine excretion was found to be significantly correlated with urine cortisol concentration (r = 0.54, P less than 0.05) and limb paresis (r = 0.52, P less than 0.05). In a multiple regression analysis, urine cortisol values were shown to be positively associated with limb paresis (P = 0.003), disorientation (P = 0.03) and body temperature (P = 0.03). High cortisol excretion was associated with a poorer functional outcome in a discriminant analysis (P = 0.001). Thus acute ischaemic stroke is associated with an increased activity in the cortisol axis. This may have a number of negative effects on organ functioning, and is a predictor of a poorer functional outcome.

Surveillance of urinary thiocyanate concentration after epidemic spastic paraparesis in Mozambique.

A large epidemic of spastic paraparesis in Mozambique during a drought was attributed to cyanide exposure from cassava. Active surveillance in one of the villages most affected by the epidemic detected four new cases in the first year after the epidemic, and none in the second year. In apparently healthy schoolchildren in the same village, surveillance of urinary thiocyanate concentration, an indicator of cyanide exposure, showed high peak values of 1175 and 673 mumols l-1 in succeeding years, with a gradual return to near-normal values in the third year. A marked seasonal variation in thiocyanate concentration was present, with the highest value coinciding with the dry season, the period of the epidemic, and the cassava harvest. Lower values were found in the neighbouring unaffected semi-urban centre. As cassava cultivation increases in many drought-affected countries, we recommend monitoring urinary thiocyanate concentration to estimate cyanide exposure and identify populations at risk for spastic paraparesis epidemics.

Two cases of acute toluene intoxication.

Two patients exposed to high concentrations of toluene in air (greater than 7000 mg/m3) were found at the bottom of a small swimming pool under construction. Their symptoms were stupefaction, paresis, and amnesia. Patient A had been exposed for three hours and patient B for two hours. Ninety minutes after the exposure, the toluene blood concentration in patient A was 4.1 mg/l and in patient B 2.2 mg/l. Urinary ortho-cresol secretion was shown to be a good index of exposure to toluene. After high level exposure, urinary meta-cresol excretion may also be used to monitor toluene exposure.

[Urinary excretion of hydroxyproline in patients with ischemic stroke]. / Wydalanie hydroksyproliny w moczu chorych z niedokrwiennym udarem mózgu.

Urinary excretion of total hydroxyproline being an indicator of the metabolism of systemic collagen was determined in 104 patients with ischaemic stroke and in 45 controls. The determinations were done by the method of Prockop-Udenfried in the urine of patients after 2 days on a non-collagen diet. Increased excretion of hydroxyproline was found in the subgroup of patients with high-grade paresis or paralysis, while in the subgroup with mild paresis these results were normal. The excretion of hydroxyproline in patients with severe paralysis increased during 3-60 days after stroke and then decreased in the period from 60 days to 5 years.

Excretion of porphyrins and porphyrin precursors during neuromuscular paralysis produced by dithiobiuret.

Urinary excretion of porphyrin precursors delta-aminolevulinic acid (ALA) and porphobilinogen (PBG) and total porphyrins was measured during intoxication of rats with 2,4-dithiobiuret (DTB), a chemical which produces delayed-onset neuromuscular weakness, in an attempt to ascertain whether or not DTB poisoning in the rat would serve as an animal model of the neurologic symptoms of acute intermittent porphyria. Daily administration of DTB (1 mg/kg/day, i.p.) produced flaccid skeletal muscle weakness first detected after 4 to 5 days of treatment. Onset of skeletal muscle weakness was associated with a significant increase in urinary excretion of ALA. The excretion of PBG and total porphyrin was also increased; however, the increase was not significant. The increase in porphyrins and porphyrin precursors was due to increased urine output which coincided with the onset of neuromuscular weakness; urinary concentrations of ALA, PBG, and porphyrins were not increased by DTB. Measurements of free-erythrocyte protoporphyrin, taken after 7 days of DTB treatment, indicated a significant elevation of free erythrocyte protoporphyrin concentration. The pattern of alterations in the heme precursors associated with DTB-induced paralysis in rats is quite different from that observed in humans afflicted with acute intermittent porphyria. Therefore, we conclude that DTB-induced paralysis in the rat does not represent an accurate animal model of acute intermittent porphyria.

Urinary elimination of glycosaminoglycans during the immobilization osteoporosis of spinal cord injury patients.

Urinary glycosaminoglycans (GAGs) were measured in 47 paraplegics, six tetraplegics, and ten control subjects. In two paraplegics, the GAG rates were compared with those of hydroxyprolinuria and calciuria during one year. The GAG excretion rate found during the first five months after spinal cord injury increased significantly, up to three or four times the normal rate. No significant differences were found between paraplegics and tetraplegics. This increase in glycosaminoglycanuria parallels the previously reported increase in hydroxyprolinuria. The formation of a neurogenic paraosteoarthropathy showed the highest increase in hydroxyprolinuria. These biochemical assessments reflect the modifications in the bone matrix and cutaneous tissue associated with immobilization osteoporosis in spinal cord injury patients.

[Aminoacid levels in Werding-Hoffmann and Kugelberg-Welander diseases (author's transl)]. / Alterazioni degli aminoacidi nella malattia di Werdnig-Hoffmann: studio comparativo con la malattia di Kugelberg-Welander.

The concentration of free aminoacids in plasma and urine were estimated in 10 patients suffering from Werdnig-Hoffmann's disease of long duration. The age of the patients was between 5 and 14 years. Estimations were also made in 10 patients with Kugelberg-Welander's disease aged between 11 and 34 years. The aminoacid concentrations were estimated on samples of plasma and 24 hours samples of urine by means of chromatography on ion-exchange resins. The data obtained were compared respectively with groups of thirty and ten healthy subjects of the same age. In the group of patients with Werdnig-Hoffmann's disease a significant increase of taurine (p less than 0.001) and of glutamic acid (p less than 0.001) was found in the plasma. The urinary excretion of glutamine was increased in the same group of patients (p less than 0.001) and in the group with Kugelberg-Welander's disease (p less than 0.005). These aminoacid levels are interpreted as an expression of a reduced oxygen metabolism and increased proteolysis in the skeletal muscles in conditions of chronic denervation.